Reactive oxygen species and biomolecular double bonds

Reactive oxygen species and biomolecular double bonds refers to the chemical interaction where reactive oxygen species (ROS), such as hydroxyl radicals or singlet oxygen, attack unsaturated carbon-carbon bonds in lipids, proteins, and nucleic acids [1, 2]. This process is most prominently observed in lipid peroxidation, where ROS initiate a chain reaction in polyunsaturated fatty acids within cell membranes, leading to the degradation of membrane integrity [1, 3]. The resulting formation of reactive aldehydes like malondialdehyde can further damage cellular components and interfere with normal function [1]. While ROS are essential at low concentrations for physiological signaling and immune defense, their uncontrolled reaction with biomolecular double bonds is a hallmark of oxidative stress [2, 4]. This oxidative damage is a key pathological driver in various conditions, including cardiovascular disease, neurodegeneration, and cancer [3]. Therapeutic strategies targeting this interaction typically involve the use of antioxidants and radical scavengers to neutralize ROS before they can cause irreversible damage to vital biomolecular structures [2, 3].

Other names

Lipid peroxidationOxidative damageROS-mediated oxidationOxidative stress-induced damage

Antioxidants and radical scavengers act by donating electrons or hydrogen atoms to neutralize reactive oxygen species, thereby preventing the initiation and propagation of oxidative damage to biomolecular double bonds [2, 3].